The left ventricle of the heart pumps cyclically to deliver oxygenated blood to the body via the aorta. The cyclic pumping of the left ventricle of the heart includes a systole stage and a diastole stage, depicted in FIGS. 1 and 2 respectively.
During the systole stage, the left ventricle 1 contracts, pumping blood to the aorta 2 through the aortic valve 3. Contraction of the left ventricle 1 increases the pressure in the aorta 2, causing the aorta 2 to expand, as depicted in FIG. 1. The expansion absorbs some of the shock loading associated with ejection of blood from the left ventricle. At various points 4 along the aorta, the aorta wall may be subject to anatomical constraints restricting the ability of the aorta to expand. The systolic blood pressure is the maximum blood pressure in the aorta during the systole stage.
During the diastole stage, the left ventricle 1 relaxes and the aortic valve 3 closes to stop back flow of blood into the left ventricle 1. The left atrium 5 contracts to fill the left ventricle 1 with further blood in preparation for the next systole stage. During the diastole stage, the blood pressure within the aorta 2 reduces to what is termed the diastolic blood pressure. The reduced pressure at this stage causes the wall of the aorta 2 to recoil (contract), restoring it back to its original diameter. The blood is accordingly pumped through the aorta and into the arteries in a pulsating manner.
The ability of the aorta 2 to expand and recoil during the systole and diastole stages is dependent upon the elasticity of the aorta wall which is a result of the elastin fibres present in the aorta wall.
Systolic blood pressure progressively increases with ageing that begins in childhood until the eighth or ninth decade, whereas diastolic blood pressure tends to remain constant in the fifth or sixth decade but decreases thereafter. Consequently, the pulse pressure, being the pressure differential between the systolic and diastolic blood pressure, increases with ageing. This form of hypertension is termed isolated systolic hypertension and increases in frequency with increasing age.
Various studies have shown that elevated systolic pressure is associated with a greater risk of heart failure, stroke, and acute myocardial infarction, and that treatment of elevated systolic pressure can delay or prevent such adverse events even when diastolic pressure is normal or low.
A number of studies have also shown that, in patients over 50, there is a stronger association between adverse cardiovascular (particularly coronary) events and pulse pressure, than systolic or diastolic pressure in isolation. Accordingly, for any given systolic pressure, the diastolic pressure is inversely related to the risk of adverse cardiovascular events, possibly due to reduction in coronary perfusion with decreased diastolic pressure.
Heart failure is reported to effect 2 to 5 percent of people in Western societies aged over 65, and 10 percent of those aged over 75. It is also reported to be the leading cause of hospital admission and readmission in Americans older than 65.
The increase in systolic blood pressure with age is largely a result of stiffening of the aorta and large elastic arteries. Dilatation of the aorta/arteries is typically associated with this stiffening. The stiffening and dilatation is a result of the repetitive cyclic stress applied to the aorta wall during expansion and subsequent relaxation of the aorta. The cyclic stresses applied to the aorta wall result in fatigue, fracture and fragmentation of the elastin fibres which provide the aorta wall with its elasticity. The mechanical properties of the aorta wall gradually become dominated by inelastic collagen. The breakdown of the elastin fibres results in the aorta becoming inelastic and stiff, thereby losing its capability to restore to its original diameter after expansion during the systole stage. The aorta accordingly remains permanently dilatated.
A young, healthy ascending aorta typically has an external diameter of the order of 25 mm when subjected to normal diastolic pressure of 70 mmHg (9.3 kPa), and a wall thickness of the order of 1 mm. The diameter and wall thickness decrease from the proximal portions of the aorta to the more distal portions. Dilatation of the aorta associated with aortic stiffening may result in an increase in the external diameter of the ascending aorta at diastolic pressure to as large as 40 mm or more.
Measurement of the stiffness of the aorta has been the subject of various studies, measuring various different stiffness related properties. The measurement of pure tensile stiffness of a section of aorta, providing a Young's modulus, is not readily obtained given the non-homogeneous nature of the aorta. A common, and more meaningful, stiffness measurement is the pressure-strain elastic modulus (Ep):Ep=(dP/dD)×D                 where D=aortic diameter;        dD=change in aortic diameter;        dP=change in aortic pressure.        
The aortic stiffness is non-linear, increasing with increasing pressure, partly due to the biochemical, structural and geometric makeup of the extracellular matrix of the aorta wall, and hence the aortic stiffness at a specified pressure is measured as the tangent to the pressure/diameter curve. Stiffness can most meaningfully be measured as the average stiffness over the range of pressures experienced during physiological flow as follows:Ep=(dP/dD)×D                 where D=diastolic aortic diameter;        dD=pulsatile change in aortic diameter (systolic diameter minus diastolic diameter)        dP=pulse pressure (systolic pressure minus diastolic pressure)        
This stiffness varies greatly from subject to subject, and increases from the proximal portions of the aorta to the more distal portions. A typical young, healthy ascending aorta will have a stiffness (Ep) of about 0.41×106 dyn/cm2 (41 kPa). A stiffened ascending aorta may have an increased stiffness of up to 16×106 dyn/cm2 (1600 kPa) or more.
Aortic stiffening alters the left ventricular systolic pressure in two ways. First, there is a greater rise in pressure at the time of peak aortic flow in the systole stage as a result of failure of the aorta to expand as blood is pumped from the left ventricle. Secondly, aortic stiffening increases the pulse wave velocity in the large blood vessels. This causes pressure waves reflected from peripheral sites to return to the aorta earlier than usual, boosting pressure in the late systole stage. This early return of the reflected wave to the ascending aorta during the ventricular ejection of systole is detrimental since systolic pressure and left ventricular afterload is increased. The early return of the reflected wave also reduces diastolic pressure and the capacity for myocardial perfusion. Each of these factors results in an increase in cardiac load of the left ventricle.
The most effective means of treating, or preventing, heart failure is to reduce cardiac load either pharmacologically or mechanically. Mechanical reduction of cardiac load using intra-aortic balloon counter pulsation and ventricular assist devices have proven effective. However, intra-aortic balloon counter pulsation can only be used as a temporary treatment. Ventricular assist devices are also expensive and temporary measures.